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HCV immune evasion and regulatory T cell activation: cause or consequence?

Cellular & Molecular Immunology 2018年第5期15卷 536-538页

作者： Haijun Li Tianyang Li ian nicholas crispe Zhengkun Tu Institute of Translational Medicine the First HospitalJilin UniversityChangchunChina Department of Pathology University of WashingtonSeattleWashingtonUSA Institute of Liver diseases the First HospitalJilin UniversityChangchunChina

Hepatitis C virus(HCV)infection remains a major public health problem given that an estimated 71 million people are currently infected and 1.75 million are newly infected every *** to 85%of HCV infections become persistent and may eventually lead to chronic liver diseases,including cirrhosis and hepatocellular carcinoma.1 Immune responses play a crucial role in virus control and liver injury;however,the underlying mechanism is not completely *** chronically infected with HCV generally exhibit a weak peripheral blood T cell response against HCV,which could explain viral *** cells that play a key role in dominant immune tolerance,regulatory T(T-reg)cells suppress inflammatory responses and prevent the development of autoimmune diseases.

关键词： infected diseases consequence

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Presentation of hepatocellular antigens

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Cellular & Molecular Immunology 2016年第3期13卷 293-300页

作者： Arash Grakoui ian nicholas crispe Division of Infectious Diseases Department of Medicine Emory University School of Medicine and Yerkes National Primate Research Center Atlantal GAUSA Department of Pathology University of Washington Seattle WA USA.

The liver is an organ in which antigen-specific T-cell responses manifest a bias toward immune tolerance. This is clearly seen in the rejection of allogeneic liver transplants, and multiple other phenomena suggest that this effect is more general. These include tolerance toward antigens introduced via the portal vein, immune failure to several hepatotropic viruses, the lack of natural liverstage immunity to malaria parasites, and the frequent metastasis of cancers to the liver. Here we review the mechanisms by which T cells engage with hepatocellular antigens, the context in which such encounters occur, and the mechanisms that act to suppress a full T-cell response. While many mechanisms play a role, we will argue that two important processes are the constraints on the cross-presentation of hepatocellular antigens, and the induction of negative feedback inhibition driven by interferons. The constant exposure of the liver to microbial products from the intestine may drive innate immunity, rendering the local environment unfavorable for specific T-cell responses through this mechanism. Nevertheless, tolerance toward hepatocellular antigens is not monolithic and under specific circumstances allows both effective immunity and immunopathology.

关键词： liver hepatocytes immunity tolerance

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Hepatitis C virus core protein triggers expansion and activation of CD4＋CD25＋ regulatory T cells in chronic hepatitis C patients

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Cellular & Molecular Immunology 2015年第6期12卷 743-749页

作者： Naicui Zhai Xiumei Chi Tianyang Li Hongxiao Song Haijun Li Xia Jin ian nicholas crispe Lishan Su Junqi Niu Zhengkun Tu Institute of Translational Medicine The First Hospital Jilin University Changchun China Department of Hepatology The First Hospital Jilin University Changchun China Institute Pasteur of Shanghai Chinese Academy of Sciences Shanghai China Department of Pathology University of Washington Seattle WA USA Lineberger Comprehensive Cancer Center School of Medicine University of North Carolina at Chapel Hill Chapel Hill NC USA

CD4＋CD25＋FoxP3 ＋ regulatory T ceils （Tregs） are increased in patients with chronic hepatitis C, which may contribute to the sustained suppression of hepatitis C virus （HCV）-specific T-cell responses and viral persistence in HCV-infected individuals. We postulated that HCV core protein （HCVc） directly contributes to the expansion of Tregs in HCV-infected patients, and we provide evidence to support this hypothesis in the report. Peripheral blood mononuclear cells （PBMCs） and sera were collected from 87 treatment-naive chronic HCV-infected patients, CD4＋CD25＋ Tregs were measured by flow cytometry, and HCV RNA and HCVc levels were detected using qPCR and enzyme-linked immunosorbent assay （ELISA）, respectively. CD4＋, CD8＋, CD4＋CD25＋ and CD4＋CD25- T cells were purified from healthy donors and cultured with recombinant HCVc and Toll-like receptor （TLR） ligands. Flow cytometry was used to analyze cell proliferation, and ELISA was performed to measure cytokine production. In the 87 chronic HCV-infected patients, HCVc showed a significant correlation with HCV RNA and CD4＋CD25＋Tregs. Mechanistic studies showed that HCVc, together with anti-CD3 antibody, augmented CD4＋CD25＋ Treg proliferation, but inhibited CD4＋CD25- T-cell proliferation and IFN-γ production, in a dose-dependent and Treg-dependent manner. Moreover, unlike the TLR3 ligand （poly hC） and the TLR4 ligand （lipopolysaccharide, LPS）, the TLR2 ligand （lipoteichoic acid, LTA） and HCVc both inhibited TCR-induced CD4＋ T-cell proliferation and IFN-γ secretion in a Treg-dependent manner. These data indicate that HCVc, like other TLR2 ligands, triggers CD4＋CD25＋ Treg activation and expansion to inhibit host immune responses, which may play a critical role in viral persistence in HCV-infected patients.

关键词： CD4+CD25+ regulatory T cells HCV core Toll-like receptor

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